The major objective of this project is to develop animal models of human disease by dietary deprivation of zinc or copper. These models will be used to determine the biochemical lesion responsible for the pathology and thus elucidate the biochemical function of these nutrients. Copper deficiency in the rat results in pulmonary emphysema, cardiac hypertrophy, purpura and neuropathology simulating Parkinson's disease. Zinc deficiency results in impaired platelet aggregation, a pregnancy disease involving physiological shock with hypothermia, hypotension and excessive blood loss. Zinc deficiency also causes water imbalance and glucose intolerance. Our results suggest that the common theme to the zinc deficiency pathology is defective membrane structure and function. We postulate that impairment of receptors is the basis of the short-term zinc deficiency pathology. The specific objectives are to measure receptors function in several systems; platelets, adipocytes, and the kidney vasculature. Both the protein (sulfhydryl components) and lipid composition of membranes, such as red cell ghosts, will be determined. The role of copper in the central nervous and lung will receive major attention. Lipid composition of brain tissue will be determined in an attempt to determine the basis of the neuropathology of copper deficiency. The effect of hyperoxia on the microanatomy of the copper-deficient lung will be studied. Finally, the effect of milk components on copper bioavailability will be investigated.